Cellular senescence of RANKL+ osteoblasts and Th17 cells in severe periodontitis with occlusal trauma.

IF 3.2 2区 医学 Q1 DENTISTRY, ORAL SURGERY & MEDICINE
Yutian Wang, Masato Nakagawa, Chuyi Luo, Ryuhei Kanda, Yasuhiko Matsushima, Aki Nishiura, Yoshitomo Honda
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引用次数: 0

Abstract

Purpose: Excessive occlusal forces resulting from inadequate dental prosthesis, along with periodontal infection (PI), lead to severe periodontitis; however, the roles of senescent cells and their involvement in the mechanisms underlying this process remain unclear. Therefore, this study aimed to elucidate the roles of senescent cells and their cell types in severe periodontitis with excessive force (occlusal trauma [OT]).

Methods: To determine whether senescent cells exacerbate alveolar bone resorption, we developed a severe periodontitis rat model by inducing PI and OT and assessed the presence of senescent cells and bone resorption. Senolytics (dasatinib + quercetin [DQ]) were administered to evaluate the changes in the appearance of senescent cells and bone resorption.

Results: PI and OT + PI increased senescent cells as well as osteoclasts. Furthermore, p21 and receptor activator of nuclear factor-kappa B ligand (RANKL) co-expressing cells were observed in the OT + PI group rats, suggesting a correlation between bone resorption and senescent cells. Cell type analysis identified osteoblasts and Th17 cells as RANKL+ cells expressing p21 or p16. DQ administration reduced senescent cells and osteoclasts, thereby preventing alveolar bone resorption.

Conclusions: RANKL+ senescent osteoblasts and Th17 cells are involved in osteoclastogenesis and bone resorption. Our findings highlight a new target for the prosthetic treatment of severe periodontitis.

重度牙周炎伴咬合损伤的RANKL+成骨细胞和Th17细胞的细胞衰老。
目的:由于义齿不充分导致的咬合力过大,加上牙周感染(PI),导致严重的牙周炎;然而,衰老细胞的作用及其参与这一过程的机制尚不清楚。因此,本研究旨在阐明衰老细胞及其细胞类型在严重牙周炎伴过度受力(咬合创伤[OT])中的作用。方法:为了确定衰老细胞是否会加剧牙槽骨吸收,我们建立了严重牙周炎大鼠模型,通过诱导PI和OT来评估衰老细胞的存在和骨吸收。使用抗衰老药物(达沙替尼+槲皮素[DQ])评估衰老细胞外观和骨吸收的变化。结果:PI和OT + PI均能增加衰老细胞和破骨细胞。此外,在OT + PI组大鼠中观察到p21和核因子- κ B配体受体激活因子(RANKL)共表达细胞,提示骨吸收与衰老细胞之间存在相关性。细胞类型分析鉴定成骨细胞和Th17细胞为表达p21或p16的RANKL+细胞。DQ可减少衰老细胞和破骨细胞,从而阻止牙槽骨吸收。结论:RANKL+衰老成骨细胞和Th17细胞参与破骨细胞发生和骨吸收。我们的发现突出了严重牙周炎修复治疗的新目标。
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来源期刊
Journal of prosthodontic research
Journal of prosthodontic research DENTISTRY, ORAL SURGERY & MEDICINE-
CiteScore
6.90
自引率
11.10%
发文量
161
期刊介绍: Journal of Prosthodontic Research is published 4 times annually, in January, April, July, and October, under supervision by the Editorial Board of Japan Prosthodontic Society, which selects all materials submitted for publication. Journal of Prosthodontic Research originated as an official journal of Japan Prosthodontic Society. It has recently developed a long-range plan to become the most prestigious Asian journal of dental research regarding all aspects of oral and occlusal rehabilitation, fixed/removable prosthodontics, oral implantology and applied oral biology and physiology. The Journal will cover all diagnostic and clinical management aspects necessary to reestablish subjective and objective harmonious oral aesthetics and function. The most-targeted topics: 1) Clinical Epidemiology and Prosthodontics 2) Fixed/Removable Prosthodontics 3) Oral Implantology 4) Prosthodontics-Related Biosciences (Regenerative Medicine, Bone Biology, Mechanobiology, Microbiology/Immunology) 5) Oral Physiology and Biomechanics (Masticating and Swallowing Function, Parafunction, e.g., bruxism) 6) Orofacial Pain and Temporomandibular Disorders (TMDs) 7) Adhesive Dentistry / Dental Materials / Aesthetic Dentistry 8) Maxillofacial Prosthodontics and Dysphagia Rehabilitation 9) Digital Dentistry Prosthodontic treatment may become necessary as a result of developmental or acquired disturbances in the orofacial region, of orofacial trauma, or of a variety of dental and oral diseases and orofacial pain conditions. Reviews, Original articles, technical procedure and case reports can be submitted. Letters to the Editor commenting on papers or any aspect of Journal of Prosthodontic Research are welcomed.
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